Updating evidence role corticosteroids severe sepsis septic shock

Septic shock is characterized by uncontrolled systemic inflammation that contributes to the progression of organ failures and eventually death.

These effects likely result from interaction of the glucocorticoid and specific membrane sites [17].It is generally accepted that uncontrolled systemic inflammation is the hallmark of severe sepsis and the main contributor for the progression of organ dysfunction and death [2].Host control of inflammation involves a complex interaction between the neuroendocrine and the immune system [3,4].Proinflammatory mediators released in the inflamed sites oppose to the anti-inflammatory response, an effect that may be reversed by exogenous corticosteroids.With sepsis, via nongenomic and genomic effects, corticosteroids restore cardiovascular homeostasis, terminate systemic and tissue inflammation, restore organ function, and prevent death.Hydrocortisone should be given at a daily dose of 200 mg and preferably combined to enteral fludrocortisone at a dose of 50 μg.Blood glucose levels should be kept below 150 mg/d L.Any imbalance favoring NF-κB bioactivity will results in uncontrolled inflammation.There is ample evidence that such an imbalance may occur in conditions of sustained stress.Indeed, they occur during the few hours after exposure to a glucocorticoid and result from physical interaction between the monomeric G-GRα complexes and NF-κB and AP-1.Then, the nuclear transcription factors are sequestrated in the cytosol and cannot enter the nucleus, preventing the reading of genes encoding for most if not all proinflammatory mediators.

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